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Previous Volume 342:664-665 March 2, 2000 Number 9 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: The review of the toll-like receptors (TLRs) by Modlin et al. (June 10 issue)¹ contained some important errors. The authors contend that TLR2 signals the presence of endotoxin, and thus alerts the host to invading gram-negative bacteria. This is wrong. TLR4 carries out this function. The genetic evidence is categorical. Animals lacking TLR4 do not respond to endotoxin and have increased susceptibility to overwhelming gram-negative sepsis.² Animals without TLR2, in contrast, have a completely normal response to both endotoxin and gram-negative bacterial infection.³ These facts cannot be reconciled with the claim that TLR2 transmits the lipopolysaccharide signal. . . . [Full Text of this Article]

References

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• Tanaka, M., Yanagihara, I., Takahashi, H., Hamaguchi, M., Nakahira, K., Sakata, I. (2007). The mRNA expression of fatty acid amide hydrolase in human whole blood correlates with sepsis. Innate Immunity 13: 35-38 [Abstract]  
• Sylla, B. S., Murphy, K., Cahir-McFarland, E., Lane, W. S., Mosialos, G., Kieff, E. (2000). The X-linked lymphoproliferative syndrome gene product SH2D1A associates with p62dok (Dok1) and activates NF-kappa B. Proc. Natl. Acad. Sci. USA 97: 7470-7475 [Abstract] [Full Text]